scholarly journals Intracerebral Transplantation of Bone Marrow-Derived Mesenchymal Stem Cells Reduces Amyloid-Beta Deposition and Rescues Memory Deficits in Alzheimer's Disease Mice by Modulation of Immune Responses

Stem Cells ◽  
2009 ◽  
pp. N/A-N/A ◽  
Author(s):  
Jong Kil Lee ◽  
Hee Kyung Jin ◽  
Shogo Endo ◽  
Edward H. Schuchman ◽  
Janet E. Carter ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Immune Responses ◽  
Amyloid Beta ◽  
Memory Deficits ◽  
Intracerebral Transplantation

Therapeutic effects of melatonin-treated bone marrow mesenchymal stem cells (BMSC) in a rat model of Alzheimer's disease

2020 ◽  
Vol 108 ◽  
pp. 101804
Author(s):  
Mahdi Ramezani ◽  
Alireza Komaki ◽  
Nasrin Hashemi-Firouzi ◽  
Keywan Mortezaee ◽  
Nafiseh Faraji ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Rat Model ◽  
Therapeutic Effects ◽  
Model Of Alzheimer’S Disease ◽  
Marrow Mesenchymal Stem Cells

Efficient Processing of Alzheimer's Disease Amyloid-Beta Peptides by Neuroectodermally Converted Mesenchymal Stem Cells

2010 ◽  
Vol 19 (5) ◽  
pp. 629-633 ◽  
Author(s):  
Hans-Jörg Habisch ◽  
Benjamin Schmid ◽  
Christine A.F. von Arnim ◽  
Albert C. Ludolph ◽  
Rolf Brenner ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Amyloid Beta ◽  
Amyloid Beta Peptides ◽  
Beta Peptides ◽  
Efficient Processing

Potential of bone marrow mesenchymal stem cells in management of Alzheimer's disease in female rats

2014 ◽  
Vol 38 (12) ◽  
pp. 1367-1383 ◽  
Author(s):  
Ahmed M. Salem ◽  
Hanaa H. Ahmed ◽  
Hazem M. Atta ◽  
Mohamed A. Ghazy ◽  
Hadeer A. Aglan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Female Rats ◽  
Marrow Mesenchymal Stem Cells

scholarly journals Exposure of Mesenchymal Stem Cells to an Alzheimer’s Disease Environment Enhances Therapeutic Effects

2020 ◽  
Author(s):  
Sang eon Park ◽  
Hyeong Seop Kim ◽  
Soo Jin Kwon ◽  
Min-Jeong Kim ◽  
Suk-joo Choi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Cell Death ◽  
Mesenchymal Stem Cells ◽  
Amyloid Beta ◽  
Therapeutic Effects ◽  
Human Mscs ◽  
Sequencing Data ◽  
Ubiquitin Conjugate

Abstract BackgroundMesenchymal stem cells (MSCs) have emerged as a promising tool for the treatment of Alzheimer’s disease (AD). Previous studies suggested that the co-culture of human MSCs with AD in an in vitro model reduced the expression of amyloid-beta 42 (Aβ42) in the medium as well as the overexpression of amyloid-beta (Aβ )-degrading enzymes such as neprilysin (NEP).MethodsIn this study, we focused on the role of primed MSCs (human Wharton's jelly-derived mesenchymal stem cells (WJ-MSCs) exposed to an AD cell line via a co-culture system) in reducing the levels of Aβ and inhibiting cell death. ResultsWe demonstrated that mouse groups treated with naïve MSCs and primed MSCs showed significant reductions in cell death, ubiquitin conjugate levels, and Aβ levels, but the effects were greater in primed MSCs. Also, mRNA sequencing data analysis indicated that high levels of TGF-β induced primed-MSCs. Furthermore, treatment with TGF-β reduced Aβ expression in an AD transgenic mouse model. ConclusionAD environmental preconditioning is a promising strategy to reduce cell death and ubiquitin conjugate levels and maintain the stemness of MSCs. Further, these data suggest that human WJ-MSCs exposed to an AD environment may represent a promising and novel therapy for AD.

scholarly journals Exposure of Mesenchymal Stem Cells to an Alzheimer’s Disease Environment Enhances Therapeutic Effects

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Sang Eon Park ◽  
Hyeong Seop Kim ◽  
Soo Jin Kwon ◽  
Min-Jeong Kim ◽  
Suk-joo Choi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Cell Death ◽  
Mesenchymal Stem Cells ◽  
Amyloid Beta ◽  
Therapeutic Effects ◽  
Human Mscs ◽  
Sequencing Data ◽  
Ubiquitin Conjugate

Mesenchymal stem cells (MSCs) have emerged as a promising tool for the treatment of Alzheimer’s disease (AD). Previous studies suggested that the coculture of human MSCs with AD in an in vitro model reduced the expression of amyloid-beta 42 (Aβ42) in the medium as well as the overexpression of amyloid-beta- (Aβ-) degrading enzymes such as neprilysin (NEP). We focused on the role of primed MSCs (human Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) exposed to an AD cell line via a coculture system) in reducing the levels of Aβ and inhibiting cell death. We demonstrated that mouse groups treated with naïve MSCs and primed MSCs showed significant reductions in cell death, ubiquitin conjugate levels, and Aβ levels, but the effects were greater in primed MSCs. Also, mRNA sequencing data analysis indicated that high levels of TGF-β induced primed-MSCs. Furthermore, treatment with TGF-β reduced Aβ expression in an AD transgenic mouse model. These results highlighted AD environmental preconditioning is a promising strategy to reduce cell death and ubiquitin conjugate levels and maintain the stemness of MSCs. Further, these data suggest that human WJ-MSCs exposed to an AD environment may represent a promising and novel therapy for AD.

Therapeutic effect of mesenchymal stem cells in an animal model of Alzheimer’s disease evaluated by β-amyloid positron emission tomography imaging

2020 ◽  
Vol 54 (9) ◽  
pp. 883-891
Author(s):  
Bok-Nam Park ◽  
Jang-Hee Kim ◽  
Tae Sung Lim ◽  
So Hyun Park ◽  
Tae-Gyu Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Standardized Uptake Value ◽  
Emission Tomography ◽  
Positron Emission ◽  
Β Amyloid

Objective: We evaluated the effects of bone marrow–derived mesenchymal stem cells in a model of Alzheimer’s disease using serial [18F]Florbetaben positron emission tomography. Methods: 3xTg Alzheimer’s disease mice were treated with intravenously injected bone marrow–derived mesenchymal stem cells, and animals without stem cell therapy were used as controls. Serial [18F]Florbetaben positron emission tomography was performed after therapy. The standardized uptake value ratio was measured as the cortex standardized uptake value divided by the cerebellum standardized uptake value. Memory function and histological changes were observed using the Barnes maze test and β-amyloid-reactive cells. Results: Standardized uptake value ratio decreased significantly from day 14 after stem cell administration in the bone marrow–derived mesenchymal stem cells–treated group ( n = 28). In contrast, there was no change in the ratio in control mice ( n = 25) at any time point. In addition, mice that received bone marrow–derived mesenchymal stem cell therapy also exhibited significantly better memory function and less β-amyloid-immunopositive plaques compared to controls. Conclusion: The therapeutic effect of intravenously injected bone marrow–derived mesenchymal stem cells in a mouse model of Alzheimer’s disease was confirmed by β-amyloid positron emission tomography imaging, memory functional studies and histopathological evaluation.

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